The life span of individuals that are sero-positive for human immunodeficiency virus
(HIV) has greatly improved; however, complications involving the central nervous system (CNS)
remain a concern. While HIV does not directly infect neurons, the proteins produced by the virus,
including HIV transactivator of transcription (Tat), are released from infected glia; these proteins
can be neurotoxic. This neurotoxicity is thought to mediate the pathology underlying HIVassociated
neurological impairments. Cocaine abuse is common among HIV infected individuals,
and this abuse augments HIV-associated neurological deficits. The brain regions and pathophysiological mechanisms that
are dysregulated by both chronic cocaine and Tat are the focus of the current review.